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Arthur T. Suckow, PhD, became CEO of DTx Pharma through a path that taught him what he needed for this position, but before he took the title, he had to prove to himself that he was ready. A recently completed Series B financing of $100 million and a growing team of executives are solid evidence that he in fact was.
In this episode, Dr. Suckow tells host Firas Rahhal, MD, how his time spent working at Johnson & Johnson, AstraZeneca, and Regulus Therapeutics gave him the inspiration, and the different pieces of the puzzle that he needed, to focus his attention on the challenge of drug delivery, specifically using fatty acids.
He explains the work DTx is doing with small interfering RNA (siRNA) on the delivery of RNA therapeutics, and explains that fatty acids can bind to albumin, which can be used as an “Uber” to maintain exposure of drugs over prolonged periods of time.
DTx is first developing a treatment for retinitis pigmentosa, but Dr. Suckow said, “I’ve been a drug hunter my whole career,” and the company will be looking to develop products for other indications both in and outside of the eye.
Click “play” to hear Dr. Suckow talk about all this and much more!
Firas Rahhal: Welcome back, everyone to the OIS Retina Podcast. This is again Firas Rahhal of Retina Vitreous Associates here in Los Angeles and also ExSight Ventures in New York. And I have today as my guest, a good friend of mine and a colleague, Dr. Artie Suckow, who is the CEO of a company known as DTX Pharma, we’re going to hear a lot about that today already has a long history in biomedical sciences. He has a PhD from UC San Diego, in biomedical sciences and pharmacology. He’s an expert in this area. Obviously, we can’t wait to hear about some of the science that they’re doing. And he, I think, is the co-founder or the founder of the company, Artie. First of all, welcome. Thank you for coming on the show with me.
Arthur: Well, thank you for having me Firas.
Firas Rahhal: Tell us about your own personal background. You it’s I read from some of the aspects of your bio that you had previous positions with AstraZeneca, Johnson and Johnson both very famous right now they’re in the news a lot of for maybe different reasons. Although you can share with us if there’s any overlap, and Regulus something I’m not familiar with Regulus therapeutics. And again, you had previously received a doctoral degree from UCSD in biomedical sciences, pharmacology. Tell us a little bit about some of those previous positions. And were you working at that time with the fatty acid molecules and the peptides conjugated to fatty acids as I read about?
Arthur: Yeah, so maybe I’ll start. Well, it’s interesting how things come full circle. So I did my undergrad at University of Delaware. And I actually did ophthalmic research at University of Delaware, to be honest with you, I thought that was the last time I would do research in the eyes instead of the cornea. But anyway, come come to you know how I came to know fatty acids. You know, did my PhD at UCSD and in diabetes, I studied pancreatic islets insulin secreting cells went to Johnson and Johnson state in the diabetes space. From there, like you said, AstraZeneca. Again, diabetes space. The difference between J&J and AstraZeneca was J&J was small molecules. AstraZeneca was biologics like antibody, you know, antibodies, peptide conjugates. And then, you know, miss San Diego, you know, the beautiful weather in San Diego and joined a company called Regulus Therapeutics and, and that’s where I came to know the problem that DTX works on delivery of RNA therapeutics. But it was really, you know, work that I had been involved in it at J&J in working on fatty acid receptors for small molecule diabetes drug at work at AstraZeneca. Looking at fatty acids is a mean to means to project protract, the half life of peptide diabetes drugs that that sort of served as the inspiration for DTX.
Firas Rahhal: So that the work at Regulus was with RNA therapies, and that did involve these long chain fatty acids at the time, too. What were you doing there? Exactly?
Arthur: Yeah, so no fatty acid work, really at Regulus. So Regulus was, there’s all sorts of flavors of RNA therapeutics. And they worked on micro RNA, which is kind of nature’s siRNA. And it regulates many different processes. But but it was there, I was in charge of sort of thinking about new ways to deliver these medicines, it turned out that they went on under went a lot of change. And throughout my year there, I worked on CNSI, diabetes and Nash, as well as delivery. So that’s probably more reflection of the change going on there. But what I came to know, there was the delivery challenge with RNA therapeutics that has sort of plagued the space for, you know, over 30 years, right, cells don’t take these molecules up at all, and they’re rapidly cleared by the kidney. And so, you know, outside of like local indications, like the eye have been rapidly clear by the kidney precludes exposure to like heart muscle where there’s lots of opportunities for RNA medicines, but if you can’t get them there, you know, how are they going to work?
Firas Rahhal: So when you were Regulus, you’re working in the RNA therapy space, but they weren’t specific, like you are now working on a niche area of delivery of the molecules. That’s something you observed in the challenges in doing the work itself.
Firas Rahhal: Is that How the genesis of DTS came about. Tell me about how these positions ended up leading you to where you are now and how you, it led you to form GTX.
Arthur: Yeah, there’s, there’s lots, lots to this story. You know, part of it is, you know, why did I even want to start a company to begin with to part of it? How did the Genesis
Firas Rahhal: because you’re masochistic.
Arthur: I do go back and think about what I was thinking three years ago, kept me going from day to day from time to time. But anyways, you know, the genesis of DTX is kind of, you know, twofold. And maybe I’ll start with, why did you know, why was I inspired to start a company, and sort of my career path and what, you know, what I was thinking as I was at AstraZeneca, and J&J. And then what you know how DTX came. And so it turned out while I was in grad school, there’s something called the minor proposition, you have to come up with your own idea outside of you know, whatever your thesis work is. And so I presented that idea to my committee. And, you know, shortly thereafter, the, you know, one of the advisors and said there was investment group that was interested in investing in this idea, totally unrelated to DTX, but ended up getting funded and became a lab that I worked in that was outside of the university that I reduced to, to practice. And so what I realized pretty quickly there, even though the idea worked, was that, you know, having two years of experience at grad school was not sufficient to build a biotech company. But so I stored it in the back of my mind that or I mean, it sort of became my ambition to get appropriate experience in drug development. So one day, I could come back and do that, and so finished grad school. But, you know, while I was at J&J and AstraZeneca, I was always, you know, trying to interact with, you know, people far smarter than me who had more experience to learn all about different aspects of drug development. It was kind of why I moved from large pharma to biotech was, you know, Regulus, I, maybe aspirationally thought that I’d learn how to build a biotech, you know, do you know relationships, raise money, etc. Obviously, that didn’t work out. But fortunately, you know, I guess, for the prospects of building a business. What I did learn at Regulus was, as I mentioned, this delivery challenge, and why I thought, you know, with my colleagues, Adam and john thought that fatty acids were the solution for the delivery challenge was essentially because they killed two birds with one stone. And so, you know, every cell in your body has a mechanism to take up fatty acids. And so you could imagine leveraging those mechanisms to bring these molecules into cells. The other reason we really liked fatty acids is they were a tried and true mechanism. And I learned this at AstraZeneca, for promoting biodistribution. So there’s, there’s for multi billion dollar peptide drugs in the diabetes space, that leveraged fatty acids on the peptide were half life extension. And so what those peptides do, or one of those fatty acids do is they bind to a protein in the blood called the albumin, albumin kind of serves as an Uber to maintain exposure of those drugs over prolonged periods of time. And so that was the same fundamental problem that RNA therapy, you know, peptide therapeutics, with fatty acids did for peptide therapeutics, is, you know, the same problem, that RNA therapeutic space rapid clearance by the kidney. And so, you know, saw that as really underexplored relative to what others had done with fatty acids in the RNA therapeutic space. And, and that was sort of the inspiration for the idea gained, you know, traction with investors, you know, at least early on to reduce it to practice.
Firas Rahhal: It’s amazing. So, the fatty acid moieties have been, I won’t say commonly, but previously used to attach to peptides to increase HalfLife, say, in the circulation, does that also relate to their penetrance into cells, like you’re talking about here? Or is that strictly because of the value and phenomenon that you’ve discussed?
Arthur: Yeah, in that context, it’s all about they’re not, the drugs don’t need to get into cells per se. Okay, you’re trying to get them two cells to interact with like the insulin receptor, or, you know, you know, or that there’s another drug called GLP. One that’s important for promoting insulin secretion and beta cells. So So in that context, those success stories are really about Keeping drugs in circulation longer.
Firas Rahhal: Did you have exposure to this fatty acid concept while you were a grad student? Is that when you first thought about it was it later on after you saw the challenge in RNA technologies entering cells that it came to you that this might be useful there?
Arthur: Yeah, I don’t, I definitely never thought. I mean, I never thought that I would use fatty acids again, either. I mean, when I left J&J, we worked on these these fatty acid receptors for diabetes, you know, the fatty acids were ligands for these receptors, you know, wrote a paper and a review article, I thought that was the end of my career in fatty acids into, you know, AstraZeneca, you know, where we use fatty acids on peptides for half life extension, again, thought that was the end. fatty acids. And then, you know, when I saw that, that, you know, the setback in RNA therapeutics was delivery. I sort of reminisce on my experiences at J&J and AstraZeneca. And say, Man, it just seems like there’s probably a way you can, there’s, I didn’t necessarily know the exact confirmation or configuration, but it seemed like, you know, as a reasonable hypothesis as any, that this could work. And so yeah, and so, and grad school, had, there was nothing, I never even thought about drug development in any meaningful way.
Firas Rahhal: You’re too humble to say, but it seems to me as a simple guy. That’s how great scientists come up with great science, that story is a great story of how one puts together two pieces of a puzzle that are remote from one another in time and space. And this is, this is how great ideas come about, you deserve a lot of credit for that, would you say this is novel, to attach the, these moieties to RNA technology is just the first DTX in you the first of its kind, I will
Arthur: I won’t claim that we are the first company to attach fatty acids to siRNAs or antisense oligos. People have tried it since you know 2006. You know what I think it maybe is, in some ways, there’s a fortunate coincidence of cross fertilization here. Having seen this in other contexts, that it seemed obvious to me that that folks had tried to attach fatty acids to siRNAs, and tried all different ones, but sort of didn’t, you know, have the same appreciation that we brought to the space of how they actually interact with receptors and albumin to be able to leverage that, that knowledge. So, you know, people tried, you know, you probably have, everyone’s probably heard of cholesterol, right? People tried attaching cholesterol, and it worked reasonably well. But, you know, cholesterol hasn’t been safely deployed for anything, whether peptide or otherwise, so that that didn’t work out. And you’ll even see, you know, publications all the way through last year of people attaching a single, fatty acid, you know, so the idea of using fatty acids is by no means novel, I think what we, you know, brought to the table was a, you know, we had conviction that fatty acids were the solution. And we more aggressively pursued, you know, different numbers, orientations, lens, all different kinds of variables, the way I kind of think about it, honestly, is like, small molecule drug development, right, you get a hit. It’s like a one micromolar hit, it barely binds, it’s active. And so that’s kind of what were the field was, you know, when we came to the scene, and then we did SAR, more chemistry, to optimize the way those are presented to cells and to make, you know, orders of magnitude improvement. So that’s, I guess, that’s the way that the incremental benefit that we brought to the space.
Firas Rahhal: I understand. So that brings me right to the topic I want to move into, which is the company of course, that you founded. It’s called DTx, start by me because I’ve never known this, even though for the audience, I’m an investor at through ExSight, our group is one of the investors in your company. How did you come up with the name? DTx? What does it mean?
Arthur: Yeah, this is kind of it’s you’re gonna get a kick out of this. So
Firas Rahhal: I’ve been dying to ask you actually, this case, this gave me an excuse to ask you.
Arthur: So there’s multiple there’s multiple answers to this. So I think the honest answer is the first 100 names we came up with maybe more because I remember the email conversations between the founders. Were all you know, either taken from a website perspective To where we couldn’t afford the domain. So, I guess we ultimately settled for Delivery Technologies. So that’s what the D T stands for. And then where you’re going to kick get a kick out of this is the x actually comes from, you know, when I was younger and I had Instant Messenger, I used to use the x as spaces between initials in my screen name. And so my screen name was Michael Jordan, x, MJ x SP x, Dr. Scottie Pippen, Dennis Rodman, and the access basis. So DT was taken. So we added the x as, the space, you know, what was cool about the x on the logo being almost immediately you could imagine building like a little siRNA off of the x. So you got to be careful what you ask for in the answer to the question.
Firas Rahhal: That’s a great, that’s a great answer. It’s very honest, it could have easily been DT underscore given. Given I like gx By the way, x’s. And Z’s, are very popular with the Madison Avenue drug name developers, the guys who, because I did this as a resident for extra money. When I was a resident in New York City back in the very early 1990s. They’d have focus groups, and they would want to name drugs, many of them are out on the market now. And sure enough, 20 years later, I saw these glaucoma drugs coming out that had Z’s and x’s in them, because these Madison Avenue gurus knew that would be catchy-ish. And it really, if you take a look at an inventory of ophthalmology, eye drops in the commercial world, a lot of them have x’s and Z’s. So you did well by the the Madison Avenue guys would have agreed with you. So let’s talk a little bit about the technology. It’s fascinating. At the same time, it’s complicated, it’s hard for some of us regular folk to understand it. It’s siRNA and for everyone listening, small interfering RNAs. Tell us a little bit broadly and as simplistically, as you feel you can deliver the message. What does this mean? How does the siRNA work? What What, what is the therapeutic effect that might be gained by using this technology?
Arthur: Yeah, so my simplistic way of, you know, explaining this is, you know, DNA, you’ve got the code, the DNA, that DNA, you know, is it’s almost like a cookbook, it’s it’s, it’s transcribed into a message. And then the message results in a protein that does all the work. And so the way RNAs drugs work or siRNAs work, is they essentially chop up the message, right, they cleave it, they clip it, they make sure that there’s not going to be any message around. And then therefore, that prevents the expression of the protein. And so why do you want to get rid of the protein? And so there’s lots of, you know, we hear about mutations and genetics. And so there’s mutations in genes that lead to proteins that are toxic to cells, or take on functions that that you don’t want. And so by, you know, intercepting the message, or preventing the expression of the message, you can prevent the expression of the disease causing protein. And I don’t, maybe it’s helpful, because this is an eye, you know, podcast, I could use an example gene like rhodopsin, right? We know, in retinitis pigmentosa, for example, mutations in rhodopsin, lead to blindness. And so in this case, you know, you use an siRNA therapeutic to get rid of the mutant rhodopsin to prevent the disease. So are present prevent, you know, retinitis pigmentosa. So I hope that I broke it down simple enough.
Firas Rahhal: No, it makes a lot of sense the way you propose it, which is ultimately the protein is the product. And along the way, you’re breaking up the messaging system, the building system. So this is going to block the formation of proteins, you would never use it in reverse to try to create a new protein that’s better. That’s a different form of gene therapy.
Arthur: Right? Yeah, exactly. So that’s, um, so broadly speaking, RNA therapeutics, it also encompasses what you’re suggesting kind of replacing the mRNA and it’s, it’s timely, because, you know, that’s the mRNA technology is what you know, Moderna and Pfizer using for the COVID-19 vaccines.
Firas Rahhal: Excellent. That’s very clear. It and for some of my listeners who’ve been around for a while treating ophthalmology patients since the 90s. I’ll bring up a product that maybe you can comment on this. As you mentioned, this has been a concept sort of circulating biomedical space for 30 years in ophthalmology, we did have some brief experience with it in the 90s. I believe it was in siRNA, but it may have been something called anti sense. And if there’s a difference, maybe you can help us what those differences are, the product was called later, I think commercially, fulmar verson, it was used for CMV retinitis, I knew the person who developed it helped to develop the New York a great clinician at Mount Sinai. And I was treating a lot of CMV retinitis in the 90s. And this was fairly popular as it came on. But it didn’t have didn’t last too long and may have been because CMV as a disease kind of diminished away with much better HIV treatment. Do you know about that drug? And what was that? Exactly? And what’s the difference, if any, between siRNA and Antisense?
Arthur: Yeah. So maybe I’ll start with the latter part of the question, which is there are, you know, as you kind of elucidate that there are different flavors of, you know, Gene suppressing RNA therapeutics. And so there’s siRNA that I just described. And then there’s, and, you know, if we get into the, you know, hardcore molecular biology, the difference between siRNAs, they work in the cytoplasm, the Antisense molecules, they work within the nucleus. And so that’s a fundamental difference. They just use different, you know, protein complexes to accomplish the same end to chop up, you know, to get rid of the the message. And so, maybe coming back to vitruvian, I think you actually answered the question on what happened to that drug, it went extinct because of heart therapy. And, you know, I think it was I’m blanking on the name, who was it? In any case, whoever what was withdrew marketing authorization in 2004 and 2006, because there was no market to sell the drugs to any you know, any more. I guess other probably other points related to you know, siRNAs versus Antisense. Our enthuiasm, for siRNAs, maybe I’ll start there as is they’re, they’re quite a bit more potent, you know, anywhere from 100 to 1000 fold more potent than an ASO to accomplish the same end, repressing repression of gene expression, they also have a really long duration of action following a single injection, they can last as much as a year, which is obviously really attractive when we talk about the eye. And then one other, you know, maybe this is going into the weeds a bit, but I think your audience will be very familiar with some of these drugs is Antisense. Not only can it can be used to repress the expression of genes, but can also do something called exon skipping. And you’ll you know, you’ll you’ll have heard of many of these drugs, I’m sure you’ve heard of pro qR, they’ve got a product for retinitis pigmentosa for LCA. And the reality is, you know, those are exon skipping is where Antisense has Shawn. And so I’ll actually defer to you on whether you want me to take a stab at explaining exon skipping, or whether we want to move to another another topic, but just you know, there’s lots of flavors of these things. They can accomplish different things. for different purposes.
Firas Rahhal: I actually would like to hear but I’m gonna let it go. Because I know you could do it well, and everyone would understand it. But I want to get into some of the clinical stuff that you and I talked about. It is more familiar to me and most of the audience members, by the way, I think that company you were looking for I think it was called ISIS pharmaceuticals that brought that product to market and it was a good product. There were a lot of good products for CMV in those days. So the first I indication for your product in the Eyespace, again, is retinitis pigmentosa if I’m if I’m correct. How did you come to this and specifically within that disease, what are you what are you aiming at? What’s the product that you do?
Arthur: Yeah, so we were always very interested in the eye for this class of medicines. In some ways, we viewed the eye as a good place to understand the technology without the confined confounding of facts of you know, biodistribution, or rapid clearance by the kidney, we also, you know, really like the eye. You know, because it’s a compartmentalised approach, this class has a really long duration of action on a single injection. And so I’m sure you’re familiar with all the vegf products and trying to take them from monthly to quarterly to six months to two yearly. And so we always were attracted to using RNA therapeutics, because they have that built in long duration of action. And then there’s there was also, you know, reasonably compelling advantages, versus gene therapy, in terms of, you know, the number of cells with a genetic lesion that you can access. So distribution. So, how we came to work on RP is interesting, we came across the literature through actually someone we both know, Dan Chow, on. That was, it’s an approach that’s meant to be agnostic to the underlying genetics driving the disease. And, and so, you know, we put that up against other programs in RP that would more specifically address an underlying genetic lesion. And so, you know, just, you know, demonstrated it, it worked in, you know, wild type mice, and then a couple of different, I think, three different wrote in models of the disease, and then, you know, pitted up against other projects in the company and went out to the KOLs and inherited retinal degenerations. and asked them, you know, which of these potential products are you most excited about? And in our approach to, you know, agnostic approach to the underlying genetics, driving RP, you that was unanimously selected? And so we’ve been pushing that forward ever since.
Firas Rahhal: You’re talking about the one that specifically agnostic to the genetics of the RP?
Arthur: Yeah. And I think one of the challenge is, you probably know this as well, as I do. One of the challenges with with RP is it’s, it’s genetically diverse, there’s 100 genes, 300 mutations. And it’s really hard, you know, to isolate any one of these genes and develop a drug for it, because there’s not many patients with any specific lesion and then not at a they’re not typically at a time point where intervention is likely to work. And so that’s why I think everyone was attracted to this approach that could work in more than one mutation.
Firas Rahhal: So that makes a lot of sense. And I agree with your KOLs, by the way, with the with the strategy, and we’ve talked about this, you and I. So it would be applicable to most all comers with Rp. What about applicability to say, different stages of disease? Do you think this product would be more likely to be helpful early stage disease mid or even advanced stages of bear light perception or, you know, those patients?
Arthur: Yeah, I think it’s more in the mean, the prophylactic category than sort of late stage. One of the major challenges with retinitis pigmentosa, at least as I understand it, not having studied it for my entire career is that, you know, you what happens is you have the death of the photoreceptor cells. And so, as I understand it, if you don’t have photoreceptor cells, if none of the treatments are going to be able to work. And so just by kind of definition of the disease, you have to start early to prevent the death of those photoreceptor cells, and that’s so the earlier, the better, I think, you know, would be the strategy for this particular approach.
Firas Rahhal: Yeah, I agree. Totally. I think for those really late stage disease categories, there’s different paradigms, which we won’t get into great detail on here. optogenetics is being you know, attempted there. As you know, from Second Sight, there have been some electronic, you know, devices attempted there. But for a product like yours yet, early and mid stage makes a lot more sense. Where are you with the preclinical development now of this product?
Arthur: Yeah, so we we’ve nominated, I guess, in drug development, we call clinical candidates. Now, we did that earlier this year. And so that means that we’re triggering the the, the characterization and the safety that would support first inhuman dosing, sometime in 2022. And so we’re moving through, you know, you know, monkey and Rabbits studies that would support a safety package, you know that would allow us to advance the program.
Firas Rahhal So you would be your goal would be to have start human clinical trials in 2022. With this product.
Firas Rahhal: That’s pretty near term. So you’re already doing currently? or about to do a nonhuman primates?
Arthur: Yeah. So we’re doing we’re at the dose range binding stage of our tox studies. And those are usually do those in twos, two species. And it’s safe to assume that one of those is non human primates.
Firas Rahhal: Okay. Great. That’s pretty far along. What about the corporate development? Again, for full transparency? I, as a member of ExSight, I’m an investor. So I’m aware of some of this. I’m aware that you had a great close to arrays recently. I think that’s been public. What can you tell us about that recent raise that you feel comfortable to talk about? And where do you expect that to take you and who is involved?
Arthur: Yeah, so yeah, the big announcement is we raised, you know, about a month ago, we raised $100 million. You know, from a combination of our existing early investors, as well as RACapital, Access, Janus, Cormorant, Surveyor, and Eli Lilly, who was also an, you know, an investor in our Series A, in terms of where we expect that to that capital to get us, you know, specifically with respect to the eye mean, our goal is to get into human studies with that capital, demonstrate safety and identify appropriate doses to move into, you know, studies where we would understand, you know, understand whether this is a potential mechanism to prevent the pathogenesis of Rp. Of course, that’s a lot of money, and we’re doing other things. And so, we’re working in other therapeutic areas, including neuro muscular applications of the technology, the goal is to take one of those programs into phase one, and potentially even some early proof of concept in patients there. And then, you know, we have aspirations to, you know, break open other therapeutic areas for this class of therapeutics. And, you know, we want to remain the leaders and leveraging fatty acids and so to overcome the delivery challenges in the space so you know, there’s there’s some efforts to understand it in new areas like the CNS or oncology.
Firas Rahhal: Okay, that’s I You got me to a point I wanted to get to with you. And thank you for that the other programs you’re looking at and I knew that you’re in the new neuromuscular space or or pursuing that, I didn’t know about the oncology Have you already started any work in the oncology space now is that for later?
Arthur: That I would just say, for later for now it’s on it’s on the to do list.
Firas Rahhal: What’s ruminating inside your brain, I don’t count that as now we’ll count that. That’s the now that the real stuff later I get, I glad you mentioned Eli Lilly, cuz it’s one of the things I wanted to bring up. I know, they were an early investor with you. I know, I had spoken with them in a group call, when we were, you know, doing diligence, on DTx, with you and with them. And we were very impressed with their level of knowledge and understanding of this space. We were very happy to join in the round when they came in. How’s it been having a company like that a strategic with such experience and broad wings to come in so early, there’s obviously value add, how did you view that?
Arthur: Yeah, I mean, we, you know, we’ve gotten lots of value out of that, that relationship. I mean, first and foremost, you know, for the way this company was was kind of built up, you know, from the ground up, you know, it was really important that we had external validation of what we are doing what we were doing, you know, outside of the the local San Diego ecosystem. And so, you know, by Eli Lilly taking a look at the the technology and saying this is sufficiently interesting that we’ll put some, some money behind it was really important. In our development, we also got the benefit of having their their CSO at the time of RNA therapeutics, Andrew Adams, on our board who’s you know, understand space really well. He understands how to create value in the space and it allowed us to you know, get get some insight into how, you know, potential partners, potential acquirers, you know, look at these opportunities and the data sets that that you need to take need to have to create value in the area. So I mean, you know, very significant inflection point and, and very valuable for the company to have that relationship.
Firas Rahhal: I know you’ve added some great people in recent months. And obviously, you just had this excellent race. Congratulations. Are there some corporate growth areas that you’re eyeing right now? Or are you kind of in a steady state and just going on to do more science?
Arthur: We’re definitely not in a steady state. I mean we are a data driven and R&D company. And so, you know, a good chunk of our investment is in in filling out our team with folks that are experts in ophthalmology experts in neuromuscular diseases, both internally and externally. Now that we’re bigger there are, you know, we have to build out the operations arm of the company, so we, you know, we will be looking to add a CFO and a VP of finance, clinical operations, etc. And maybe, maybe we’ve we’ve discussed this, but we brought on Denise Bevers, as our Chief Operating Officer, who, you know, has lots of experience building, building companies and taking companies public, Brian Laffitte are CSO from Novartis, and, and Chuck to lead the chemistry and he has, you know, 20 years of experience in oligo. therapeutics. So, you know, those, those folks are much more knowledgeable about all those areas than, than me are really, you know, leading the charge in terms of building out the, you know, the talent that will keep this company, remaining leaders in the space.
Firas Rahhal: And that probably means you get to take off some of the hats, but it probably it won’t reduce your workload. I know you’re a hard worker, and you’ve led this company, amazingly, where you previously functioning as the CSO, as well as the CEO, so to speak, prior to bringing in the recent folks.
Arthur: Yeah. I mean, my as you know, my I’ve been a drug hunter for my whole career. And so when, you know, when
Firas Rahhal: Be careful how we referenced that later, but
Arthur: Drug Hunter by day and night. Anyway, the Yeah, I mean, in some ways, when I when when we started DTx, John Adam, and me, I didn’t feel comfortable, you know, calling myself as CEO, because my background was really CSO background. And so, I guess, more recently, as you know, the company has grown and I’ve, I’ve had to prove myself maybe prove to myself that I was capable of doing some of the the non-science related aspects of a CEO thought, you know, I guess I feel in my own head, I transition to a CEO. But also, I think it’s really important. As you know, I spent a lot of time raising capital meeting with investors, you know, putting infrastructure in place to support the company, I thought it was important, especially with the programs to bring on someone like Brian Pena pass the baton, who, you know, has done this over and over again, more times than I’ve done it, to really, you know, take some of the, you know, or divide and conquer, I guess you could say is the best way to way to put it. So, you know, was really, you know, really enthusiastic to bring him on board to help bring these programs forward?
Firas Rahhal: Well, usually it is true that the scientist guy, which is you for sure, might have to give some thought to, can I be the CEO guy? Well, you you, I’ll say as an investor, and now your friend, you’ve done it in spades, you did train yourself in whatever way and if this recent raises improve, you know, there’s 100 million reasons that you have been able to successfully and I mean, this only half jokingly, to success, we build the infrastructure and lead the program, not just with science, but with management that people are believing in you and putting their money in for good reason. And you should be congratulated, that’s a hard thing to do to wear both of those hats and you’ve done it very well. And you’re probably pretty tired a lot. It’s one final question. Really, on the AI? We’ve had some very casual conversations you and I in the past about indications outside of RP, you mentioned the non eye stuff the neuro muscular What about in the eye other indications you’re considering?
Arthur: Yeah, I mean, we definitely are looking for, you know, other opportunities in the eye, I would say nothing has really gained traction in the way that RP has gained traction. And we’ve, you know, we’ve looked, as you know, we’ve looked across a whole host of, you know, potential opportunities, not you’re not limited to, you know, the genetic variants of RP we discussed, dry eye, uveitis, Fuchs’, wet AMD. And so you know what has limited us or our sort of prevented us from taking a shot in some of those areas is in, in part, the competitive landscape. You know, when we pick indications for DTx, I always say we, we pick indications where if we’re successful, we will win, you know, because we’re addressing either the underlying genetic lesion and we can be the first to do that. Or, you know, because, you know, the, you know, the competitive landscape and other opportunities is favorable. But we’re definitely still working through the process of identifying other opportunities in the eye. And I’m sure there’s one there that fits the criteria. We just, you know, aren’t ready to announce it just yet, or commit to it just
Firas Rahhal: that I like to be continued. We’ve gone back later as things evolve, for sure. And I mean that. Artie Suckow, Dr. Artie Suckow thank you for joining me and the rest of the team and OIS for our podcast. This has been fascinating. You’re doing a great job, you’re to be congratulated, and I appreciate you coming on.
Arthur: Thanks Firas. Thanks for having me. And appreciate all the thoughtful questions.
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